The invention concerns a device for the therapy of supraventricular and ventricular bradycardial and tachycardial disrhythmias and/or for influencing the heart pumping force.
The normal heart rate of a human being is between 60 and 100 beats per minute at rest while under a load it can rise to 180 beats per minute. A resting heart rate which is below 60 beats per minute is generally referred to as bradycardia while a resting heart rate which is over 100 beats per minute is referred to as tachycardia. Tachycardias can originate in the atria (so-called supraventricular tachycardias or atrial fibrillation) or can occur in the ventricles (so-called ventricular tachycardias and ventricular fibrillation). Bradycardias on the one hand can be the expression of a slowed rate of pulse production in the normal pacemaker center of the heart (the so-called sinus node) or can be caused by a pathological delay in transmission of the excitation from the atria to the ventricles (so-called AV-node disease). The by far most frequent supraventricular tachycardia, atrial fibrillation, occurs to an increasing extent with increasing age and is to be found in more than 5% of people who are over 65 years old. Supraventricular tachycardia results in particular by way of a reduction in the diastole time in a reduced degree of ventricular diastolic filling of the heart and thus a reduced heart time volume. Particularly in a situation involving pre-existing heart pumping weakness (so-called cardiac insufficiency), that results in arterial hypotonia (forward failure) and a back-up of blood in the lungs, which has an adverse effect on enrichment of the blood with oxygen in the lungs (so-called reverse failure). In addition the consumption of oxygen on the part of the heart rises with at the same time reduced diastolic coronary circulation.
Stimulation devices are known which influence the behaviour of the heart by stimulation and/or tachycardia termination or cardioversion. Those devices however exclusively have detection units and stimulation devices which in response to given input criteria trigger signals which act exclusively directly on the mechanical behaviour of the heart by stimulation of regions of the heart, on which the electrical activity signals which are directly related to contraction of the heart are propagated. That is disadvantageous because that means that signal events which are related to those signals that directly influence the cardiac events are not influenced.
The object of the present invention is to provide a device of the general kind set forth in the opening part of this specification, which is suitable for already involving regulating intervention in the preliminary stages of the known production of stimulation or defibrillation or cardioversion signals.
That object is attained by the features recited in claim 1.
The invention is based inter alia on the realisation that the frequency of supraventricular tachycardias can be reduced by activation of the parasympathetic autonomous nervous system and can be increased by activation of the sympathetic nervous system. The cardiac output can also be generally increased and/or reduced. A rate-increasing/decreasing action on the sinus node is referred to as a positively/negatively chronotropic action while an action which promotes/inhibits atrioventricular conduction (AV-conduction) is referred to as a positively/negatively dromotropic action.
Parasympathetic nerve fibers which innervate the sinus node, the atria and the atrioventricular nodes extend along the superior vena cava, the coronary sinus and the right pulmonary artery. Sympathetic nerve fibers which result in a rise in the sinus node and/or atrium rate and an acceleration of atrioventricular conduction extend to the stellatum ganglion by way of a dorsal nerve loop which bears from the back against the arteria subclavia (the so-called dorsal ansa subclavia) and a ventral nerve loop which bears from the front against the arteria subclavia (so-called ventrale ansa subclavia) to the cardiac muscle. The ansae subclaviae contain virtually all sympathetic nerve fibers which lead from the ganglion stellatum to the cardiac muscle. These predominantly involve pre-ganglionary nerve fibers which are changed over to post-ganglionary fibers in the ganglion cerviclae medius and the upper thoracal boundary line ganglia.
Ventricular tachycardias have similar hemodynamic changes to supraventricular tachycardias. As however in contrast to many supraventricular tachycardias a synchronised atrial contraction prior to the ventricle contraction does not occur, a ventricular tachycardia, at the same rate, is hemodynamically worse than a supraventricular tachycardia. In particular however the altered intraventricular contraction process in the situations involving ventricular tachycardia results in a marked reduction in beat volume and arterial hypotonia, which means that patients with ventricular tachycardia generally lose consciousness more quickly than patients with a supraventricular tachycardia at the same rate. In particular however ventricular tachycardias quickly degenerate into ventricular fibrillation, a condition in which the ventricles beat asynchronously and incompletely at frequencies greater than 400 beats per minute. That results in a loss in arterial blood pressure. Ventricular tachycardias and ventricular fibrillation are the main cause of so-called sudden heart death which is responsible for about 80% cardiac-related deaths per annum.
The sympathetic autonomous nervous system plays a key role in the occurrence of ventricular tachycardias and ventricular fibrillation. Thus the sympathetic neurotransmitters adrenaline and noradrenaline can trigger abnormal automaticity and ventricular extrasystoles in the infarct area or can accelerate the transmission speed through myocardium scars after a cardiac infarction, which promotes the occurrence of ventricular orbits and ventricular tachycardias.
Finally, patients after cardiac infarctions are frequently found to have areas in the cardiac muscle in which the sympathetic cardiac nerves have also perished, which causes denervation oversensitivity of those areas to adrenaline and noradrenaline. Such an oversensitivity and non-homogeneous sympathetic innervation promote the occurrence of ventricular tachycardias and ventricular fibrillation.
The parasympathetic autonomous nervous system and its neurotransmitter acetyl choline antagonise the influence of the sympathetic nervous system on the heart and can prevent sudden heart death in animal models.
Clinical testing procedures which measure the sympathetic and parasympathetic tone in patients have shown that an increased sympathetic tone and reduced parasympathetic tone significantly promote the occurrence of sudden heart death.
Parasympathetic nerve fibers which innervate the ventricles accumulate in a fat clump at the level of the coronary sinus in the region of the proximal left-hand coronary artery.
The second essential parameter having an influence on the heart time volume, besides the heart rate, is the contraction force of the heart. It describes what amount of blood is expelled per heart beat (beat volume). In addition it determines the extent and the rate of the rise in pressure in the artery upon a heartbeat. Numerous diseases which can result in a decline in heart musculature such as for example coronary heart disease with cardiac infarctions can result in a reduction in the pumping force of the heart. The result of this is that, at a normal heart rate, the pumping force of the cardiac muscle is not sufficient to permit a minimally necessary beat volume for the purposes of maintaining normal arterial blood pressure and for the purposes of preventing an accumulation of blood upstream of the heart. Influencing parameters which result in an increase in the contraction force of the heart are referred to as positively inotropic parameters. Positively inotropic actions are afforded in particular by catecholamines such as adrenaline and noradrenaline which are diffused by the so-called sympathetic autonomous nervous system as neurotransmitters.
Sympathetic nerve fibers which innervate the ventricles extend in a ventral and dorsal nerve loop around the right and left arteria subclavia. Further sympathetic nerve fibers run in a ventrolateral nerve from the stellatum ganglion and the inferior cervical boundary strand ganglion respectively along the pulmonary vein and the coronary sinus to the ventricles.
In accordance with the invention, including advantageous developments, there is provided a medical electrostimulation device for the therapy of supraventricular and ventricular bradycardial and tachycardial disrhythmias and for increasing the heart pumping force, comprising
electrodes for the electrical and/or magnetic stimulation of parasympathetic nerves which innervate the sinus node, the atria, the atrioventricular nodes or the ventricles;
electrodes for the electrical and/or magnetic stimulation of the atria and ventricles and for ventricular cardioversion/defibrillation;
a device for producing electrical and/or magnetic stimulation pulses which are passed to the electrodes;
a device for detecting the rate at which the human atria and ventricles beat, said device measuring atrial and ventricular depolarisations;
a device for detecting biological parameters such as the arterial blood pressure, the right-ventricular or left-ventricular pressure, oxygen saturation of the blood or the heart time volume, the myocardial or thoracal impedance or monophase action potentials or evoked myocardial potentials;
a device for programming a frequency limit above or below which a beat rate of the heart is identified as tachycardia or bradycardia;
a device for programming a blood pressure/heart time volume limit, below which a heart insufficiency requiring treatment is identified;
a device for programming a blood pressure/heart time volume, above which sympathetic nerve stimulation in inhibited or reduced;
a start unit which reacts to the detection unit and which activates the device producing the stimulation pulses, if the detected heart beat rate of the atria or ventricles exceeds/falls below the programmed frequency limit;
a start unit which reacts to the detection unit and which activates the device producing the stimulation pulses when the arterial blood pressure/heart time volume falls below a programmed lower limit;
the stimulation pulses can be delivered over a defined period of time continuously or as short bursts. Stimulation bursts in turn can be delivered either asynchronously or in synchronised relationship with the atrial or ventricular depolarisation. Synchronisation is then effected with a varying time delay in relation to the measured atrial/ventricular depolarisation in the atrial/ventricular refractory time;
a unit which compares the atrium/ventricle frequency measured during stimulation by the detection units and the arterial blood pressure and the heart time volume to the corresponding values prior to/without stimulation and the corresponding programmed limit values; and
a stimulation unit which can provide for atrial and/or ventricular electrical and/or magnetic myocardial stimulation or cardioversion/defibrillation.
For electrical and/or magnetic stimulation of parasympathetic nerve fibers which are to reduce the atrium frequency in the event of supraventricular tachycardias and/or which are intended to slow down the ventricle frequency in the event of supraventricular tachycardias electrodes are implanted in the superior vena cava, the inferior vena cava, in the right atrium, in the coronary sinus, in both jugular veins, the right or left vena anonyma or the pulmonary artery.
Electrodes are implanted in the coronary sinus for electrical and/or magnetic stimulation of parasympathetic nerve fibers which are to prevent or terminate ventricular tachycardias/ventricular fibrillation.
For electrical and/or magnetic stimulation of parasympathetic nerve fibers which innervate the sinus nodes, electrodes are implanted in the jugular veins, the superior vena cava, the lateral right atrium in the region of the intersection of the pulmonary veins or in the pulmonary arteries.
For electrical and/or magnetic stimulation of sympathetic nerve fibers which are to increase the heart rate or the pumping force of the heart, electrodes are implanted in the right and/or left arteria subclavia or vena subclavia or the pulmonary veins or the coronary sinus.
The stimulation electrodes can be fixed intravascularly or extravascularly/epicardially at the identified stimulation locations. Nerve stimulation can be effected in a unipolar or bipolar mode, in which case the bipolar reference electrode can be part of the nerve stimulation electrode or part of a second nerve stimulation electrode implanted in the proximity of the first nerve stimulation electrode. In that respect fixing of the probes can be effected actively, for example by screw mechanisms or passively, for example by anchoring devices.
The pulse-producing device for the stimulation of autonomous nerves and for electrical and/or magnetic myocardial stimulation can involve any suitable technology for the production of stimulation pulses at a frequency of between 0 and 100 Hz and a single pulse duration of between 0 and 10 ms. The pulses can be monophase or biphase.
By virtue of a modification in the pulse-producing unit, instead of or in addition to electrical pulses, it is also possible to produce alternating magnetic fields in the pico to xcexc-tesla range, which are delivered to the nerves and/or the myocardium by way of suitable electrodes which involve appropriate coil structures.
Nerve stimulation is typically implemented at 20 Hz with a pulse duration of between 0.1 and 4 ms.
When the situation involves ventricular tachycardia, short bursts (typically between 10 and 50 ms in duration) of high-frequency individual pulses are delivered immediately after ventricular depolarisation (R-blip) in order to avoid ventricular myocardial depolarisation during stimulation of the parasympathetic nerves along the coronary sinus. Likewise stimulation of the ventrolateral nerve which extends close to the atrial/ventricular myocardium is preferably effected in bursts (typically between 10 and 50 ms in duration) of high-frequency individual pulses which are delivered immediately after ventricular depolarisation (R-blip) in order to prevent ventricular myocardial depolarisation during nerve stimulation.
The electrodes for detection of the atrial/ventricular frequency are disposed in the atrium/ventricle and are connected to an adjustable signal amplifier which amplifies the detected signal to varying degrees, depending on the respective signal magnitude. The band pass properties of the filter of that amplifier are optimised for the detection of atrium/ventricle depolarisations. The mode of operation of the amplifier/filter can correspond to that of known atrium/ventricle pacemakers.
With the measures according to the invention, it is possible to indirectly influence the heart rate by comparison of the current heart rate with one by way of a physiological parameter (activity parameter) for the heart output requirement by sympathetic or parasympathetic stimulationxe2x80x94depending on whether the current heart output is just exceeding or is below the current requirement. That occurs in contrast to previous rate-controlled pacemakers in which the desired stimulation rate was set by direct stimulation of the heart muscle at the corresponding rate.